Bleomycin (BLM)-induced mouse pulmonary fibrosis is a commonly used model in IPF research [6,15]; in vivo studies showed that a suppressed or down-regulated NF-κB signaling pathway could attenuate BLM-induced pulmonary fibrosis [13–18], while in vitro studies also found that the NF-κB signaling pathway contributed substantially to the regulation of TGF-β, a critical inflammatory mediator in myofibroblast proliferation and EMT [13–18]. This evidence concerns the gene TGFB1 and pulmonary fibrosis.